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Mechanism of Disease > Mechanism of Cell Death > Flashcards

Mechanism of Cell Death Flashcards

1
Q

Define

Etiology

A

Cause of a disease

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2
Q

Define

Pathogenesis

A

Biochemical and molecular mechanisms of disease development

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3
Q

Define

Morphology

A

Appearance of cells/tissues/organs

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4
Q

Define

Clinical Features

Manisfestation

A

Functional consequences of mophological changes

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5
Q

Lungs filled with fluid and bacteria.

What is the morphology? What are the clinical features? What is the disease?

A

Morphology: Fluid filled lungs
Clinical Features (functional consequence): Reduced gas exchange, shortness of breathe

Pneumonia

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6
Q

Why do cells die?

A

Lack of resources
Exposure to toxins
Removal of aging/ineffective cells
Attack by immune system

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7
Q

What are some events that can cause cell death due to lack of resources?

A

Hypoxia
Nutrient Deficiency
Growth factor withdrawal

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8
Q

Cellular Level: Signs of injury?

A

Intracellular accumulations
* Fatty deposits
* Lipofuscin
* Protein

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9
Q

Modes of Cell Death

Unregulated - Necrosis Signaling

Pathological

A

Cell breaks down/explodes and contents are released

Amount of signlaing depends on the cause
Spread/damage neighboring cells

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10
Q

Modes of Cell Death

Regulated - Apoptosis (multiple)

Physiological

A

Cell disassembles and packages contents for phagocytosis

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11
Q

Alternative Modes of Cell Death

Other modes besides regulated and unregulated

A

Necroptosis (regulated necrosis)
Anoikis (detachment-induced cell death)
Ferroptosis

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12
Q

What is the difference between stressed tissue and necrotic tissue?

A

Stressed: Blebbing, Eosinophilia, Swelling; staining variation, nuclei cluster, cells swell/rupture
Necrotic: Loss of Nuclei, Breakdown of membranes; cells have ruptured

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13
Q

What are the types of Necrosis?

A

Coagulative
Liquefactive
Caseous
Fibrinoid

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14
Q

Types of Necrosis: at tissue level

Coagulative

A

Loss of cell architecture but not tissue architecture

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15
Q

Types of Necrosis: at tissue level

Liquefactive

A

Digestion of cells results in viscous mass

Cells gone but more liquid

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16
Q

Types of Necrosis: at tissue level

Caseous

A

Fragmented cells and granular debris surrounded by inflammation

Cells gone but more solid

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17
Q

Types of Necrosis: at tissue level

Fibrinoid

A

Immune complexes and fibrin inwalls of blood vessels

Fibrin from blood gets in blood vessel wall, attaches to immune complex

Very eosinophilic staining

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17
Q

Causes of Necrosis

A

Overwhelming Damage
* Toxins
* Excessive Calcium
* Damage to ER and mitochondria
* Reactoe Oxygen Species (ROS)
* Ischemia
* Membrane damage
* Nutrient Withdrawl

Cells just fall apart

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17
Q

Specific instances of physiological cell death:

Immune Function

A

Destruction of elf-reactive lymphocytes to prevent autoimmunity
Death of cells that have served their purpose
Pyroptosis

Neutrophils die after an acute inflammatory response
Lymphocytes die at the end of an immune response
Pyroptosis - overreaction of caspases during immune function can result in cell death

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17
Q

Specific instances of physiological cell death:

Embryogenesis

origin of programmed cell death

A

Death of specific cells at specific times

During digit development

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17
Q

Apoptosis: Programmed Cell Death

Specific instances of physiological cell death:

A
  • Embryogenesis
  • Tissues that prduce new cells as part of their function
  • Loss of hormone-dependent tissues when hormone levels fall
  • Immune function
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17
Q

Specific instances of physiological cell death:

Tissues that produce new cells as part of their function

A

Immature lymphocytes in the bone marrow and thymus that fail to express useful antigen receptors
Epitherlial cells in intestinal crypts, so as to. maintain a constant number (homeostasis)

17
Q

Specific instances of physiological cell death:

Loss of hormone-dependent tissues when hormone levels fall

A

Endometrial cell breakdown during the menstrual cycle
Ovarian follicular atresia in menopause

17
Q

Apoptotic Initiators

A
  • Viral infections
  • Ionizing radiation
  • Chemical damage to cells
    *** Cytokines (TNF, Fas, ligand)
  • Mitochondrial damage**
  • UPR
  • Calcium influx
  • Unresolved stress
17
Q

Major morphological features of apoptosis

A
  • Cell rounding/condensation
  • Nuclear condensation/fragmentation
  • Membrane Blebbing
  • Formation of apoptotic bodies

  • Nuclear condensation/fragmentation - visible with DAPI
  • Membrane Blebbing - Visible with light microscopy
  • Formation of apoptotic bodies - Packaging of cell contents into vesicles
17
Q

Apoptosis Signaling

Extrinsic starting point of Apoptosis

A

Death receptors on the plasma membrane are actvivated and transduce a signal through intracellular signaling pathways to activate caspases

Initiated by things outside of the cell

17
Q

Define

Apoptosis

A

programmed cell death
Damage but sufficent resources to manage process instead of just falling apart

18
Q

Apoptosis Signaling

Intrinsic starting point of Apoptosis

A

Mitochondrial signals induce release of pro-apoptotic proteins that activate caspases

Initiated by things inside the cell

Damage to mitochondria can initiate

19
Q

What are Caspases?

Cysteine Aspartases

A

Specific proteases that disasseble the cell
Biochemical markers of apoptosis
Consensus sequences: cleave after aspartic acid residue
Inflammatory: Involved with NFkB signaling

20
Q

Initiator Caspases

A

2
8 - extrinsic
9 - intrinsic
10 - extrinsic

21
Q

Executioner caspases

A

3
6
7

22
Q

Extrinsic Apoptotic Signaling

A
23
Q

TNF/TNFR vs. FasL/Fas

A
24
Q

Death Domain Superfamily

Four subfamilies involved in protein complex assembly:

A
  1. Death Domain (DD) subfamily
  2. Death Effector Domain (DED) subfamily
  3. Caspase Recruitment Domain (CARD) subfamily
  4. Pyrin Domain (PYD) subfamily

Homotypic binding

Proteins MUST have the same domain to bind - through homotypic binding

25
Q

Process to caspase activation

A

Initiators (autocatalytic)
Executioners (cleavage)
DED (extrinsic)
CARD (intrinsic)
Inflammation

26
Q

Intrinsic Apoptotic Signaling

A
27
Q

What are the 2 groups of the conserved domains (BH1-4) of the Bcl-2 Protein Family?

B cell lymphoma 2
Bc2 homology domains

A

Antiapoptotic BCL-2 Proteins
BH4-BH3-BH1-BH2-TM
Pro-apoptotic BCL-2 proteins
Effectors: BH3-BH1-BH2-TM
BH3 Only

28
Q

Mitochondrial Pro-Apoptotic Factors

A

Activaed by caspases through tBID

29
Q

How does tBid function as a mitochondrial pro-apoptotic factor?

A

Bid is truncated by multiple different proteases including calapins and caspases
Bid will sequester antiapoptotic BCL-2 family members or activate pro-apoptotic members (Bax and Bak)

30
Q

Apoptosome formation

A
31
Q

Types of Failed stress response

A

p53-induced cell death (DNA damage, genotoxic stress)
ER stress/UPR - halts protein translation and upregulated chaperone expression
Calcium signaling

32
Q

What is the function of p53?

anti-oncogene

A

Critical in DNA damage repair
Transcription Factor
Negative regulators of cell cycle progression
promotes apoptosis

33
Q

What happens if p53 is unbalanced?

A

Underexpression - increases cancer susceptibility
Overexpression - promotes aging

34
Q

PIDDosome

p53-induced death domain

A
35
Q

Define

ER Stress

A

accumulation of misfolded proteins

36
Q

Define

Unfolded Protein Response

A

Stress response that promotes degredation of proteins and increased chaperone production to improve folding

37
Q

How does the ER participate in death signaling?

A

Release of ER calcium can prime mitochondria (intrinsic pathway)
ER propagates death-inducing stress signals through Bcl-2 family members

38
Q

ER stress-induced cell death contributes to:

A

Fas-induced cell death (BAP31 cleavage by Caspase 8)
p53-induced cell death

39
Q

What are the effects of cellular calcium?

A

Overload of cellular calcium is a known factor of necrosis
homeostasis is effected by Bcl-2 family

40
Q

Calcium Toxicity

ER calcium depletion…

A

induces UPR

41
Q

Calcium Toxicity

ER calcium release…

A

may activate specific enzymes

Calpain (protease) - Bid/Bax/Bcl-2 cleavege; Cadpase 12 activation
Calcineurin (phosphatase) - bad dephosphorylation

42
Q

Calcium Toxicity

Excessive mitochondrial calcium…

A

Impairs mitochondrial function (depolarization)
Increased ROS generation
Induces release of proapoptic factors

43
Q
A

Mechanism of Disease (11 decks)

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